Since ERβ has already been shown to transcriptionally downregulate another G protein-coupled receptor—GPR141—to inhibit actin-based migration in inflammatory breast cancer [65], there is a possibility of functional crosstalk between ERβ and GPER or other GPCRs, where ERβ might oppose EGFR signaling by inhibiting the expression and activity of GPER. This evidence concerns the gene GPR141 and inflammatory breast carcinoma.